Introduction and aims of the study. Obesity and type 2 diabetes have been associated to bone alterations and increased risk for fragility fractures. These metabolic and bone disorders are often accompanied by an increased accumulation of Bone Marrow Adipocytes (BMAds) and immunoinflammatory alterations. However, the regulations and consequences of the increased marrow adiposity still remain unclear. The cathelicidin peptide (CAMP) of the innate immunity is a multifunctional regulator involved in inflammation and various cellular functions. Our study aimed to investigate the capacity of differentiated BMAds to express the CAMP gene under metabolic stress. Methods. Human bone marrow mesenchymal stromal cells (hBMSCs/SSCs, RoosterBio) were differentiated into BMAds for 21 days (d21) in the presence of glucose at 5.5, 11 or 25mM (to mimic hyperglycemia). The expression of the studied genes was analysed using real-time PCR. Results. The mRNA of CAMP was detected in hBMSC-derived BMAds from day-3 of differentiation, and its levels increased following the development of the adipocyte phenotype. In mature adipocytes (d21), the CAMP mRNA levels indeed displayed a marked increase (31, 15, or 16-fold, for 5.5, 11 or 25mM of glucose, respectively) as compared to d3/5.5mM glucose. However, the high glucose conditions (11 and 25mM) significantly reduce the CAMP expression as compared to low glucose/5.5mM (p<0.05). Besides, the expression of adipogenic markers, including PPARg, CEBPα, CD36, as well as the mRNA levels of the adiponectin and chemerin, two adipokines implicated in immunoinflammatory responses, were also increased in mature BMAds (d21 vs. d3, p≤0.05). Conclusions. We demonstrated that differentiated BMAds express the hCAMP gene, the expression of which appears to be regulated by metabolic stimuli. Differentiated BMAds display features of an immunoinflammatory phenotype. Ongoing studies in vitro and in obese/diabetic mice model, should clarify the mechanisms regulating the CAMP expression in BMAds and its functional relationship with bone remodeling.